Left Ventricular (LV) Thrombus
- LV thrombus is usually seen in patients presenting with large anterior STEMIs
- Late presentation is an important risk factor
- LV thrombus results from the “perfect storm” of factors contributing to “Virchow’s Triad:”
- LV wall akinesis/dyskinesia resulting in stagnant blood flow
- Pro-coagulative state
- Ischemia resulting in inflammation
- The incidence of LV thrombus is about 5-7% in anterior MI.
- (Number may be smaller with modern reperfusion times)
- Imaging options:
- Echo (most commonly used)
- CT or MRI.
- LV thrombus forms 12-72 hours after MI.
- Imaging too early in the MI course may not identify an LV thrombus
Treatment of LV Thrombus
- The most dreaded complication of LV thrombus is stroke.
- Vitamin K antagonists (VKAs)
- DOACs are available, but only used if VKA-intolerant (no clinical trials available, case reports only)
- Primary prevention in anterior MI
- CCS 2018 – No routine anticoagulation (citing poor evidence and high risk of bleeding)
- AHA 2013 – Class IIB indication for anticoagulation
- Generally treat with anticoagulation for 3-6 months, and repeat echo to reassess whether the LV thrombus has resolved.
|CCS 2018 Heart Failure Guidelines|
|AHA 2013 STEMI Guidelines|
Left Ventricular Aneurysm and Pseudoaneurysm
- Left ventricular aneurysm
- Result of thinning of the myocardium
- Identified by a large neck
- Low risk of rupture
- Persistent ST elevation on EKG
- Left ventricular pseudoaneurysm
- Cardiac myocardial rupture that is contained by the pericardium
- Very narrow neck
- High risk for rupture → increased mortality
Right Ventricular (RV) Infarct
- Complication of inferior STEMIs
- Loss of RV contractility to maintain forward flow leads to LV underfilling (reduced preload), reduced cardiac output, and hypotension.
- Drugs that further reduce preload such as nitrates and diuretics can worsen cardiac output leading to worsening hypotension and shock.
- The RV is supplied mostly by the RV branch of the RCA. A proximal RCA lesion can compromise the RV branch.
- Early recognition and diagnosis of an RV infarcts is important.
EKG Findings in RV Infarct
- Indirect evidence of RV infarction:
- ST elevation in lead III > Lead II (Suggests RCA occlusion)
- ST elevation in V1 (Remember: V1 is closest to the RV on a typical 12-lead EKG).
- ST elevation in V1 but ST depression in V2 (Suggestive of RV infarct).
- Direct evidence of RV infarction:
- ST elevation in V4R (V4 Reverse) (15-lead EKG is required). V4R puts a lead directly over the RV.
- Remember only 0.5mm of ST elevation is required to be considered positive in V4R.
- RCA lesions are most common reason for RV infarct as the RV branch is supplied by the RCA.
- Usually very proximal lesions.
- Can be useful in assessing the severity of an RV infarct
- Visual qualitative assessment
- TAPSE (Tricuspid Annular Plane Systolic Excursion) is a validated tool to assess RV function
- Involves am M-mode at the base of the RV to assess tricuspid annular motion
- Normal ≥ 1.7 cm
- TAPSE has been validated as a predictor of heart failure and survival
- Tissue Doppler
- Systolic excursion (S’) of < 9.5 cm/sec is suggestive of RV dysfunction
RV Infarct on ECHO
- Even after revascularization, the right ventricle may take some time to recover.
- Hypotension Management
- The main hemodynamic problem resulting from an RV infarction is reduced LV preload, which causes reduced cardiac output/shock and hypotension.
- Avoid therapies that further reduce preload (nitrates, narcotics, propofol, etc.)
- Use therapies to improve preload (IV fluids, vasopressors)
- Improves RV stroke volume, and improves RV afterload by reducing pulmonary vascular resistance
- Ideally used after revascularization, as inotropes can cause complications during acute MI (arrhythmias, increase in infarct size, etc.)
Inferior infarct-related heart block:
- Usually RCA, rarely can be circumflex
- Heart block associated with high-vagal tone Bezold-Jarisch reflex or rarely from AV node ischemia
- Often transient and can be treated with atropine
- Pacemaker should generally be avoided due to risk of RV perforation (can be placed in extreme circumstances)
Anterior infarct-related heart block:
- Usually related to extensive infarct and damage to the conduction system in the septum
- Complete heart block often preceded by RBBB + LAFB
- Temporary/permanent pacemaker more likely to be required; usually see more distal conduction disease like Mobitz 2, third degree heart block, or alternating bundle branch blocks
Ventricular Septal Defect
- A very uncommon complication of acute MI.
- Typically seen in late-presenting patients who have not been revascularized. They are often female, older patients, and have no history of MI/Angina prior to presentation (less collaterals).
- Often have poor prognosis.
- Anterior Infarct often located at the apical ventricular septal.
- Inferior Infarct often located at the inferobasal ventricular septum. Usually a worse prognosis.
- Prominent pan-systolic murmur at left lower sternal border often associated with a thrill.
- Signs of right sided heart failure, pulmonary edema or shock.
- Echo helps confirm evidence of a VSD with left to right shunt as well as complications such as RV failure.
- Hemodynamic support with ionotropes, afterload reduction with nitroprusside and can consider IABP for mechanical support as bridge to surgery
- Surgical closure or percutaneous options
- Uncommon complication but very high mortality.
- The risk factors are similar to VSDs: patients are often older, late-presenting, female, first presentation MI (lack of collaterals)
- Patients can have sudden PEA arrest from cardiac tamponade
- Myocardial rupture is typically preceded by pain similar to the patient’s initial presentation
- Hypertension, excessive straining, coughing, or vomiting may be triggers
- Cardiac Arrest → Standard ACLS plus pericardiocentesis
- Hemodynamic compromise → Fluids, dobutamine/pressors, pericardiocentesis
- Traditionally, pericardiocentesis was discouraged in patients with myocardial rupture due to concern of worsening hemorrhage into the pericardial space. However, pericardiocentesis (with removal of only 10-50 mL) is still sometimes performed in patients with extreme hemodynamic instability to improve hemodynamics until definitive surgical management is delivered.
- Surgical consultation is a must. Teflon or pericardial patch can be performed on the epicardium to stabilize the rupture.
Papillary Muscle Rupture
- Pulmonary edema
- Murmur: may not be very loud because of rapid equalization of pressures across the mitral valve, but patients will have severe MR
- Posteromedial papillary muscle
- Most common
- Single blood supply PDA
- Anterolateral papillary muscle
- Dual blood supply from the LAD and circumflex artery
- URGENT surgical consult
- Primary Author: Dr. Daniel Durocher (MD FRCPC)
- Dr. Pavel Antiperovitch (MD, FRCPC)
- Perri Deacon (medical student)